| A central hypothesis that cranial suture growth and modeling vary with respect to the mechanical loading environment is tested in a mouse sagittal suture model using three Specific Aims. Experiments within these aims were designed to elucidate mechanisms of bone formation and bone resorption at the cellular level and to determine how these processes influence the morphology and performance of cranial suture connective tissues. It is argued that suture waveform complexity (measured using fractal analysis) is generated by the positive coupling of osteogenesis along convex bone margins and bone resorption along concave bone margins and that this turnover cycle is regulated in large part by mechanical forces acting on the suture bone-ligament interface. This suture form-function relationship is believed to operate via mechanosensing mechanisms within skeletal connective tissues. Although mechanically-induced cell wounding appears to be involved in normal suture biology, it does not occur in the fashion predicted. Apoptosis is not directly implicated. Thus, it is predicted that bone resorption in cranial sutures does not localize according to regions of shear-induced cell death but rather to regions adjacent to osteoblastic activity. Tension rather than shear is most likely to be the driving force in this system. |
